Mucoid otitis media is characterized by thick and visco-elastic effusions in the middle ear that reflect high concentrations of mucins. It is one of the most common otologic diseases in children and can ultimately scar the middle ear and lead to persistent hearing loss and communication problems. There is increasing evidence that mucoid otitis media results from the acute forms of otitis media along a continuum. The pathogenesis of this continuum is not well understood, but most likely involves the alteration of mucin metabolism. We proposed to investigate the pathogenic mechanisms of mucoid otitis media focusing on the alteration of mucus cell metaplasia and mucin gene expression as the key events leading to this transition. We will identify factors that modulate gene expression and mucus cell proliferation using primary culture or rat middle ear epithelial cells and experimental models of otitis media. Identifying the triggers that create the transition of acute to chronic otitis media may enable us to develop a noel therapeutic strategy to interrupt these triggers and stop the pathogenesis of this continuum.